Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001993301 | SCV002230691 | pathogenic | Fanconi anemia | 2021-11-24 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Trp15*) in the FANCC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FANCC are known to be pathogenic (PMID: 17924555). This premature translational stop signal has been observed in individual(s) with breast cancer (PMID: 32427313). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV004043989 | SCV005032526 | pathogenic | Hereditary cancer-predisposing syndrome | 2023-11-22 | criteria provided, single submitter | clinical testing | The p.W15* pathogenic mutation (also known as c.45G>A), located in coding exon 1 of the FANCC gene, results from a G to A substitution at nucleotide position 45. This changes the amino acid from a tryptophan to a stop codon within coding exon 1. This alteration was observed in 2/5054 African American women with breast cancer (Palmer JR et al. J Natl Cancer Inst, 2020 Dec;112:1213-1221). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Baylor Genetics | RCV004571701 | SCV005057604 | likely pathogenic | Fanconi anemia complementation group C | 2024-03-14 | criteria provided, single submitter | clinical testing |